marasmus- 1985 - postgraduate medical...

Postgraduate Medical Journal (1985) 61, 915-923

Marasmus- 1985

D. Barltrop and B.K. Sandhu

Department ofChild Health, Charing Cross and Westminster Medical School, London, UK.

Introduction

Dr Wilfred J. Pearson writing for the first volume ofthis Journal in 1925 defined marasmus (Greek: maras-mos, wasting) as 'a chronic state of malnutrition of asevere grade' but pointed out that 'we must retain theconception ofcases varying in severity from those whosimply show an insufficient gain or stationary weightwith few systemic changes, to the most extreme formwhich is merely the end result of repeated nutritionalor constitutional disturbances.' He described oedemain some cases as a complication of marasmus. Theclinical picture of the syndrome, later described askwashiorkor, was not generally recognized at thistime, although a number of authors had described it(Czerney & Keller, 1928).

In 1933 Cicely D. Williams, a paediatrician workingin the Gold Coast of Africa described a 'nutritionaldisease ofchildhood associated with a maize diet' andattributable to protein deficiency. She named it kwa-shiorkor (taken from the Ga language of Ghana, thedisease ofthe deposed baby when the next one is born).Her classical description included oedema, chiefly ofhands and feet, wasting, diarrhoea, irritability anddermatosis. This paper attracted much attention in themedical literature and clinical descriptions of similardisease subsequently appeared from many other coun-tries. Paradoxically the more commonly encounteredtype of malnutrition, marasmus, was neglected anduntil recently did not attract detailed scientific inves-tigation.The original view that kwashiorkor resulted from

protein lack in the presence of adequate, even excesscarbohydrate, in contrast to marasmus which foll-owed deficiency of energy alone, is not now accepted.Thus it has been shown that the protein: energy ratioof diets eaten by children developing washiorkor isadequate but total energy is deficient (Rutishauser &Frood, 1973; Goplan, 1968). However, it has becomeapparent that malnutrition produces a spectrum ofsyndromes ranging from simple growth failure aloneto both pure and mixed syndromes of marasmus,marasmic kwashiorkor and kwashiorkor.

In 1959 Jelliffe coined the term protein-caloriemalnutrition (PCM) of early childhood to includemild, moderate and various types of severe degrees ofmalnutrition. The advent of the International Systemof Units (SI) resulted in the introduction of the termprotein energy malnutrition (PEM). The WorldHealth Organisation (WHO, 1973) defined PEM asfollows: 'A range of pathological conditions arisingfrom coincidental lack, in varying proportions, ofprotein and calories, occurring most frequently ininfants and young children and commonly associatedwith infection'. This is not dissimilar from WilfredPearson's view of marasmus.

In order to treat and, more importantly, to prevent acondition effectively, evolution and causes must beunderstood. It is therefore necessary to considermarasmus within the context ofPEM. The aim of thispaper is to review the current state of knowledgeconcerning the pathophysiology, aetiology, clinicalpresentation and treatment of marasmus in the con-text of it being considered as one of a spectrum ofsyndromes produced by severe protein energy mal-nutrition (PEM).

Classification

Although a methodology for the assessment ofPEM isneeded, it is still not clear exactly what should beassessed, and there is a lack of agreement aboutclassification among experts in this field. Until recent-ly the method of classification used was that in-troduced in 1942 by Gomez and his colleagues (1956)based upon weight for age, in which the weight of thechild was expressed as a percentage of the expectedweight of a healthy child of the same age using a localor other appropriate standard (Table I).A Wellcome working party (1969) considered the

classification of PEM and agreed that the termmarasmus should be applied to children who have lessthan 60% of the expected weight for age and nooedema i.e. Gomez's severe or 3rd degree malnutri-tion. However Gomez's method assumed that childrenof any given age should have the same weight and thisassumption is incorrect. In 1972, Waterlow published

© The Fellowship of Postgraduate Medicine, 1985

Correspondence: D. Barltrop, M.D., F.R.C.P., WestminsterChildren's Hospital, Vincent Square, London SW1P 2NS,UK.

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916 D. BARLTROP & B.K. SANDHU

Table I Classification of PEM (Gomez, 1956)

Severity % ofstandard (Harvard)normal > 90%mild (1st degree) 89-75%moderate (2nd degree) 74-60%severe (3rd degree) <60%

Table H Classification of PEM according to wasting andstunting (after Waterlow et al., 1972)

Stunting Wasting(height for age) (weight for height)0=>95% 0=>90%1 = 95-90% 1 = 90-80%2 = <90-85% 2 = 80-70%3=<85% 3=<70%

0 denotes normal, and 1, 2, and 3, mild, moderate and severePEM.

a classification based on both weight and height (TableII). He labelled present malnutrition 'wasting'measured by loss of weight related to height; and pastmalnutrition 'stunting' seen in retarded height for age.This system is now generally accepted and in 1977,WHO published recommendations primarily basedupon it (Waterlow et al., 1977). However, it needs to betranslated into simpler terms for use in the busyroutine clinic.

Other anthropometric measurements such as mid-arm circumference, skinfold thickness, mid-arm andhead circumference ratio have been used but re-producibility is poor for the first two and there is anage limitation for the third.

Prevalence

Despite considerable research, UN resolutions anddevelopment programmes, there is more malnutritionin the world now than existed 30 years ago (Latham,1982). There is an increasing gap between the people ofthe rich and poor nations and there has been a failureto reduce malnutrition and hunger due to poverty. Thereasons for the failure of development and for in-creased inequality are beyond the scope of this paper.

Point prevalence figures for PEM collected byWHO (Bengoa, 1974) based on 77 surveys suggestedthat about 100 million children throughout the worldare suffering from moderate or severe PEM at any onetime. The relative prevalence of marasmus and kwa-shiorkor worldwide is not known but marasmusranged up to 95% or more of cases of severe malnutri-tion in Beirut (McLaren, 1966) and Santiago (Monck-eberg, 1966).

In the UK 3rd degree PEM is rare and is usuallysecondary to some underlying organic disease but mayoccasionally be due to child abuse.

Clinical presentation

This will vary with the degree and duration of PEM,the age of the child and the presence of associatedvitamin, mineral and trace element deficiencies. Inorder to prevent marasmus it is important that theseearly changes are understood and recognized. PEM ofall degrees is most common in the post-weaning phase(9 to 24 months of age) but can occur at any age.Failure of breast feeding and inadequate artificialfeeding can lead to marasmus in the first 9 months oflife.

Mild PEM

The main clinical presentation of mild PEM is that offailure to thrive with retarded physical growth anddevelopment revealed by anthropometric abnor-malities. There is also an increased risk of infectionand retardation ofmental development. Anaemia maybe present; activity is diminished and the hair aroundthe temples may be sparse.Anthropometric abnormalities include: (1) cessa-

tion or slowing of weight gain or weight loss; (2)slowing or cessation of height gain; (3) normal ordiminished weight/height ratio; (4) decreased mid-armcircumference; (5) delayed bone maturation and (6)normal or diminished skin fold thickness.Weight and height are the most useful indices

providing that the age of the child is known. Patternsof growth failure, however, vary considerably andchronic disease, apart from nutritional deficiency,may also contribute to the problem.

Children with mild PEM have a high rate ofinfection particularly with gastroenteritis, measles andpneumonia. In tropical areas the risk of contractingmalaria, hookworm and schistosomiasis is also in-creased and it is therefore important to assess thenutritional status of any child presenting with aninfection or infestation. Both the morbidity andmortality due to infestations are considerably in-creased in children with PEM (Scrimshaw & Behar,1961; Chandra, 1983).Severe form ofPEM - marasmus

The presenting features are gross failure to thriveaccompanied by irritable crying or apathy. The childhas a shrunken, wasted and stark appearance due toloss of subcutaneous fat. The fontanelle, if present,may be sunken due to dehydration and the eyes appearlarge. There is marked wasting ofthe buttocks and the

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abdomen is usually distended. The degree ofwasting isextreme and, by definition, the child is less than 60%of expected weight for age and may be well under40-50% of expected weight. In chronic cases lengthmay also be markedly affected so that the weight/height ratio may be unaltered. In acute cases the childis grossly underweight for height; skinfold thickness,mid-arm circumference and chest/head circumferenceare all markedly reduced. The child may be anorexicbut may be ravenously hungry. There is usuallychronic, watery diarrhoea but the stools may be semi-solid; vomiting may be a feature in some cases. Thechild is listless and physical and mental development isretarded. The child may be anaemic and may havesigns of rickets.

In pure marasmus, the signs ofkwashiorkor such asoedema, dermatosis, scarcity and dyspigmentation ofhair, angular stomatitis, and cheilosis are not present.Children with marasmic kwashiorkor weigh less than60% of expected weight but, in addition, have one ormore signs of kwashiorkor.

PathophysiologyThere are marked changes in amount and distributionof body water, fat, minerals and total body protein.Total body water (TBW)There is gradual increase in TBW as a percentage ofbody weight. There is a direct relationship betweenweight deficit and total body water content (Hansen etal., 1968) and hence children with most marked tissuewasting have the greatest TBW. Increase in TBW isassociated with a proportionate rise in extracellularfluid (ECF) but children with oedema have more ECFthan those without.

Minerals

There is a decrease in total body potassium of theorder of 10-33% (Garrow et al., 1965). In addition topotassium loss with nitrogen, potassium is lost in thediarrhoeal stools resulting in a cellular deficit. Mann etal. (1972) using a 4K counting technique have shownthat total body potassium is of the order of 39 mmol/kg in marasmus, 31mmol/kg in kwashiorkor and45-55 mmol/kg in normal controls. There is depletionof other minerals. Total body sodium, calcium andphosphorus are depleted to 93%, 77%, and 79% ofexpected values (Garrow et al., 1965).

Body fat

Normally fat constitutes around 19% of body weight.In marasmus this may fall to around 5% and a high

proportion of the residual fat (up to 50%) may be inthe liver (fatty liver) although there is no relationshipbetween liver and subcutaneous fat. In the liver the fat,mainly triglycerides, first appears in the periportalarea and then spreads to the central vein area anddistends the liver cells. Fatty liver is thought to resultfrom a combination of increased flux of fatty acidsfrom adipose tissue together with decreased hepaticsynthesis of beta-lipo-proteins which normally trans-port triglycerides from the liver. The lipo-proteinsynthesis is especially sensitive to lack of protein andthe liver changes are more marked in kwashiorkorthan marasmus. On recovery the excess fat disappearsfrom the liver over about 3 weeks and usually there isno residual damage unless infection or hepatic toxinsare involved.Absorption of fat and fat soluble vitamins is usually

impaired, although steatorrhea does not usually occurin PEM. The following play a role in the pathogenesisof fat malabsorption: (a) reduced intestinal transittime; (b) impaired micellar solubilization of lipids dueto abnormalities in bile acid metabolism caused bychanges in the bacterial flora of the upper gut (Sch-neider & Viteri, 1974); (c) impaired intraluminaldigestion due to low pancreatic lipase; (d) abnormaltransport ofdigested lipids due to decreased beta-lipo-protein. In contrast to marasmus, the body fat inkwashiorkor may be well preserved.

Body protein

Children withPEM have a greater deficit of total bodyprotein than body weight compared to normal chil-dren of the same height. In severe cases total bodyproteinmay be reduced to around 50%; muscle mass isparticularly reduced and may be as low as 30% ofnormal (Montgomery, 1962) with a relative increase ininterstitial collagen and reduction in cellular protein/DNA ratio.

Protein metabolism

In severe PEM there is marked hypoalbuminaemiaand total albumin mass may be reduced by 50%. Thisoccurs despite reduction in albumin catabolism (re-duced by half) and is due to the extreme sensitivity ofalbumin synthesis to protein intake and particularlylack of the branched chain amino acids, leucine,isoleucine and valine (Waterlow & Alleyne, 1971).There is net movement of albumin from the extravas-cular to the intravascular pool so that the former isrelatively more depleted.Gamma globulins are not affected by PEM. Protein

digestion, although slightly reduced, is adequate des-pite depression of pancreatic exocrine secretion; pan-creatic P cell function may also be depressed althougha cell function and glucagon secretion are normal.

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Absorption of nitrogen from a milk diet may bereduced by 10-20% compared to normal (from 90%to 70%-80%). Nitrogen retention, however, is muchmore efficient and remains high during treatment untilalmost normal growth rates have been restored.

Changes in the gastrointestinal tract

Diarrhoea is a major problem in malnutrition and thetwo together have been estimated to cause over 5million deaths among children every year (Rohde &Northrup, 1976). A vicious cycle is establishedwhereby a child who is malnourished and more proneto infection gets repeated attacks of gasteroenteritis or

protracted diarrhoea which result in further malnutri-tion. The pathogens responsible for the diarrhoeainclude rotavirus, enteropathogenic and enterotox-igenic E.coli, salmonella, shigellae, Giardia lamblia,Entamoeba histolytica and campylobacter. The path-ogenesis of the protracted diarrhoea is rather complexand in addition to enteric infection other factors mayplay a part including the following.

(a) Lactose intolerance Many studies have shownthat, in PEM, disaccharidase levels are reduced,lactase being the most severely affected, and may below or absent in two thirds of the children. Thepathogenesis of enzyme changes is not fully under-stood but may represent mucosal damage or decreasedproduction due to protein deficiency. In severe casessucrose and glucose intolerance may occur. Afterclinical recovery lactase levels may not recover fullyalthough the child may tolerate milk feeds.

(b) Abnormalsmall bowel mucosa The mucosal chan-ges may range from almost normal villi to severe

villous atrophy with only convolutions or ridges beingvisible on microscopy. Shiner et al. (1973) found thatin PEM there are gross epithelial cell changes with abrush border which is sparse and has markedlyshortened microvilli. The nuclei were found to beirregular, the mitochondria disrupted and cytoplasmicorganelles showed a lack of organization. Biopsiesoften show intense mucosal and submucosal infiltra-tion by lymphocytes and plasma cells. On treatment,recovery of the jejunal mucosa may be slow and takemonths before it is complete. It is now established thatin the small intestine villi are the site of absorption ofsolute and water and the crypts are the site ofsecretion. In children with PEM who have a protrac-ted secretory diarrhoea the altered villus to crypt ratiomay play a role.

(c) Unconjugated bile acids Infestation or contamin-ation of upper gastrointestinal tract (GIT) with bac-teria may lead to deconjugation of bile salts. Jejunal

aspirates of children with PEM have been found tocontain unconjugated bile acids (Gracey et al., 1973).Unconjudated bile acids are known to be smallintestinal secretagogues and may play a role in thepathogenesis ofprotracted diarrhoea in these children.

Immunological changes

Infection, particularly with Gram negative organisms,is very common in severe PEM, particularly of thegastrointestinal, respiratory and urinary tracts andmay lead to septicaemia. The patients may not exhibitclinical signs of infection such as fever. Children withPEM have been found to have evidence of depressedcell mediated immunity (CMI) as measured by skintests and lymphocyte transformation and may alsoshow thymic atrophy (Smythe et al., 1971; Lomnitzeret al., 1976). Secretory IGA may be reduced and mayplay a role in infections of gastrointestinal and res-piratory tracts (Reddy et al., 1976).Serum immunoglobulins are usually normal but

antibody response to specific viral or bacterial antigenmay be impaired (Faulk et al., 1974), with obviousimplications for immunization programmes. Live bac-terial or viral vaccines may be more immunogenic (andhence effective) than killed ones. It has been suggestedthat for optimum response, immunization program-mes should be preceded by a food supplementationprogramme.The total white cell count is usually normal but

neutrophil function abnormalities have been des-cribed (Rosen et al., 1974; Sbarra et al., 1974).

All components of serum complement except C4may be reduced.

All these abnormalities are reversed with treatmentand recovery.

Central nervous system changes

Apathy and irritability are well known features ofsevere PEM and may be related to low brain potas-sium but the effect on long term intellectual develop-ment has not been established. Animal experimentssuggest that inadequate nutrition in early life can havea permanent effect on brain size and cell number. Inhumans the adult number of neurones are alreadypresent at mid-pregnancy and in order to have anyeffect PEM would have to be present from earlypregnancy or for a long time in order to affect glialmultiplication and myelinization (Dobbing, 1974).However the brains of children dying in the first yearof life with severe PEM have shown reduction in thenumber of brain cells in the cerebrum (WHO, 1974).Clinical studies also give conflicting results as socialfactors cannot be completely excluded (Grantham-McGregor et al., 1980; Lopez et al., 1985).

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Endocrine changes

The endocrine glands, particularly the adrenals andthe pituitary, appear to atrophy in PEM (Trowell etal., 1954) although there is no significant reduction inproduction of hormones. Thyroid function remainsnormal although thyroid function tests may be alteredby the alteration in plasma protein binding. Thyrotro-phin response is normal. Growth hormone level isnormal and may even be supranormal in marasmus.

Circadian oscillations are abolished but plasmacortisol level may be elevated and as hypoalbumin-aemia leads to reduced binding of cortisol, the level offree cortisol in the plasma may be particularly high.This may contribute to the abnormal glucose tolerancefound in patients with marasmus. After an oralglucose load insulin secretion may be low but returnsto normal after 3 to 6 weeks of therapy.The raised plasma cortisol diverts free amino acids

from tissue turnover to muscle rather than liver and adifferential rise in plasma cortisol may be an impor-tant difference between marasmus and kwashiorkor(Lunn et al., 1976).

Aetiology

Severe malnutrition leading to marasmus may stemfrom inadequate food intake, malabsorption, or poorutilization. However, more than one factor may beresponsible and infection, particularly of the gastroin-testinal tract, often plays an important role in thepathophysiology of the condition.PEM is much less common in adults because they do

not need protein for growth. In most normal adultsdietary protein provides only 10% of the energyrequirements.

Inadequate food intake

Marasmus, together with other forms of PEM, iscommon in areas of the world with insufficient food,inadequate knowledge of feeding techniques and poorhygiene. It has been estimated that 100 million chil-dren under four years of age suffer from moderate orsevere malnutrition (Bengoa, 1974). A recently grow-ing problem has been the importation into developingcountries of inappropriate western models such asfeeding with manufactured infant milks which havetended to replace the traditional practice ofprolongedbreast feeding. However, family incomes may beinsufficient to buy adequate supplies of milk andfacilities to prepare uncontaminated feeds may beinadequate. This is thought to have resulted in in-creased infant morbidity, malnutrition and mortality.During the nineteenth century in the industrial

towns of Europe and North America, marasmus

resulting from poor diets and numerous infectionscontributed to high infant death rates which werecomparable to those now encountered in many Asian,African and South American towns today. Urbaninfluences, rapid successive pregnancies, early wean-ing, unsound artificial feeding, poor hygiene andrepeated infections all play a role in the pathogenesisof marasmus. The reason for early weaning may bedue to another pregnancy or to the belief that the milkof a pregnant mother is harmful for the child.The reasons for inadequate food intake in the UK

are given in Table III. Anorexia and feeding difficul-ties may complicate any illness, operation or injury inchildren. There may be associated vomiting anddiarrhoea. In addition, metabolic expenditure may beconsiderably increased with negative nitrogen balanceparticularly in post-operative cases. The three factorsof impaired intake, malabsorption and increased lossof dietary nutrients often coincide in gastrointestinaltract disease.

Malabsorption

Arateus, in the second century B.C. noted that un-digested food might appear in the stools and that

Table m Causes of inadequate nutrition in the UK

ExampleSystemic diseases renal or hepatic

failure, chronicinfections, congenitalheart disease

Structural or severephysiological gastroesophagealabnormalities of the reflux, pyloricgastrointestinal tract stenosis, Pierre-

Robin syndromeNon-accidental maternal orinjury environmental

deprivation,emotionaldeprivation and/orphysical injury

Psychosomatic such as anorexiadisorders nervosa, bulimiaFood fadsEconomicdeprivationNeurological cerebral palsydisordersOthers drugs such as digoxin

and diuretics maycause vomiting oranorexia

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malnutrition could thus occur. He called this the'coeliac disease of chronic nature' (Adams, 1856).

In 1888 Samuel Gee described the clinical featuresof coeliac disease and recommended withdrawal offlour from the diet: a good example of a gut disorderleading to malnutrition and on occasions marasmuswhich is reversible on withdrawal of dietary gluten.

Table IV Causes of malabsorption

ExampleSurgical

Pancreaticinsufficiency

Mucosal smallintestinal damage

Intestinal infections

Extraintestinalinfections

Immune deficiencystates

Abnormal bileacid metabolism

Post-enteritissyndromeInflammation andinfiltration

MalignancyVenous orlymphaticobstructionSelective inbornerrors of absorptionand digestion

Miscellaneous

short gut syndrome,post gastrectomy,Hirschprung's disease

cystic fibrosis,Schwachmann-Dia-mond syndrome,chronic pancreatitiscoeliac disease,acquired lactoseintolerance, cows'milk proteinintolerance

persistent bacterialor viral infection,parasitic infestation,e.g. Giardia lamblia,enterocolitis

urinary tractinfections, recurrentrespiratory tractinfections, congenitalinfections, e.g.cytomegalovirussevere combinedimuno-deficiencyileal disease orresection, bacterialcolonization of smallintestine

following episode ofacute gastroenteritisCrohn's disease,ulcerative colitis,amyloidosislymphomasconstrictivepericarditis

glucose-galactosemalabsorption,congenitalchloridorrhoealethal familialprotracted diarrhoealaxative abuse

Other causes of malabsorption, defined as the failureofthe normal digestive and absorptive functions ofthesmall intestine for at least one nutrient (Burke &Anderson, 1975), are given in Table IV.

Children presenting with protracted diarrhoea poseparticular problems in diagnosis and management.The diarrhoea may be devastating and the childseverely marasmic. The diarrhoea may result from awide variety of aetiologies but in a small proportiondiagnosis cannot be made despite extensive investiga-tions (Larcher et al., 1977; Sandhu & Milla, 1984).

Treatment

The present day treatment of marasmus has evolvedover the years and as our understanding of thepathophysiology ofPEM has improved the treatmenthas become more scientifically based.

Treatment of severe PEM can be divided into threephases:- resuscitation, stabilization and rehabilita-tion. During stabilization, if the underlying aetiologyis not apparent, investigations may need to be under-taken to establish a diagnosis. In the developingcountries the exact treatment used will depend on thelocal facilities and resources available and variousregimes incorporating locally available food sourceshave been described (De Meyer et al., 1981; Harland,1983; Vis, 1985).

Resuscitation

The immediate causes of death in severe PEM aredehydration and electrolyte imbalance, infection, hy-poglycaemia and hypothermia and these need urgentattention. Dehydration usually needs to be correctedwith an intravenous isotonic solution. If the child hashypovolaemia the ideal initial fluid may be plasma orblood (20 ml/kg). If intravenous therapy is not availa-ble rehydration may be carried out using an oralglucose-electrolyte solution.The child needs to be nursed in a warm room as

marasmic children are susceptible to hypothermia.Infection may be present without pyrexia and if thechild appears septicaemic or critically ill, antibioticsneed to be given after blood cultures and otherbacteriological specimens have been obtained.

Stabilization

During this phase of initiation of recovery, mainten-ance amounts of energy and protein are graduallyintroduced and a steady state achieved (0.6g ofprotein and 95 cal/kg/day). Too rapid an introductionof protein may produce liver failure and coma, toohigh an energy or sodium intake may lead to cardiacfailure. Oral feeding is usually started as frequent

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small boluses ofmilk, the first few feeds may be diluted1:1 with water. If there is lactose malabsorption, a

lactose-free formula is usually necessary. The maras-

mic infant is prone to prolonged non-specific diarr-hoea. In children who have severe protracted diarr-hoea and temporary multiple food intolerance, theusual practice in the UK is to use an oligoallergenicformula consisting of comminuted chicken with car-

bohydrate added as a glucose polymer (Francis, 1974).Gradually long chain fatty acids, triglycerides,vitamins and mineral supplements are added. Alter-natively a formula based on a casein hydrolysate, maybe used or introduced after the child has beenstabilized on a comminuted chicken mix.

If there is not a rapid response to dietary manipula-tion and the child continues to lose weight, parenteralnutrition is normally started at an early stage and maybe life saving. Otherwise a vicious cycle with persistentdiarrhoea, and failure to replace depleted tissues willpredispose to overwhelming infection, septicaemiaand death. The only way to interrupt this cycle is toprovide adequate energy and protein intravenously.The intravenous solutions contain amino acids, dex-trose, electrolytes, minerals and vitamins. The amountgiven is gradually increased and a fat emulsion can beadded to the regime.

In the less developed countries peripheral alimenta-tion has been found to be more successful than thecentral venous route because of the high incidence ofsepticaemia associated with central venous cathetersin malnourished children nursed in poorly staffedunits unfamiliar with parenteral feeding. Peripheralalimentation may be continued for two to three weekswhile oral feeds are gradually being introduced. If thediarrhoea still poses a serious problem, particularly ifthe small intestine is in a secretory state, phar-macological agents with antisecretory properties maybe helpful (Sandhu et al., 1981, 1983).Rehabilitation

After stabilization the child is ready to start theprocess of repair and growth. This demands not onlyadequate provision of energy and protein but alsovitamins (A, B, D, C and folic acid), essential mineralsand trace elements. The energy needs for growth are

approximately 5 cal/g of tissue. A child weighing 6 kgand a weight of 60 per cent of the expected weight forhis age and height needs 4,000 x 5 = 20,000cal inaddition to maintenance for catch-up growth. Rapidrehabilitation requires 150 to 200cal/kg (Ashworth,1980). This can be accomplished using milk or milksubstitute with added vegetable oil and a diet plannedwith the help of a dietician with the child feedingaccording to appetite. The voluntary intake falls tonormal values as the expected weight for height isapproached. During rehabilitation mother-child in-

teraction needs to be encouraged and improved.Developmental delay and apathy characteristic of themalnourished child can be reversed if stimulation andplay are provided (Grantham-McGregor et al., 1980).

Prognosis

The mortality figures from various units around theworld vary considerably but it is apparent that overthe last 30 years the mortality rate from severe PEMhas decreased from approximately 50% to as low as1%. The long term morbidity will depend on theunderlying cause and the environment to which thechild returns. In the majority of cases if the environ-mental circumstances are favourable, normal statureand health can be obtained (Keet et al., 1971).Although it is often stated that malnutrition in earlylife permanently impairs intellectual development,there is little evidence to support this proposition(WHO, 1974) and environmental factors probablyplay a considerable role in the ultimate intellectualachievement of each child.

Prevention

Severe PEM is closely associated with infection and ismore prevalent where poverty, social inequality, poorhygiene and ignorance coexist. Marasmus has almostbeen eliminated in the more developed countries overthe last century due to improvements in living stan-dards, health education and improved hygiene.Similar improvements are needed elsewhere in theworld. Practical strategies to alleviate malnutritionand infection include adequate food supply, uncon-taminated drinking water, improved waste disposal,primary health care, control of communicable dis-eases, and the promotion of breast feeding. There isalso a need for the detection of mild and moderatePEM, whether due to malnutrition or underlyingorganic disease, so that the treatment can be initiatedbefore a life threatening condition has developed.Our understanding of the pathophysiology of

marasmus and other forms of PEM has increasedconsiderably over the last 50 years and the mortalitydue to severe PEM has decreased markedly. However,many fundamental questions, such as why a child withsevere PEM may present with marasmus and anotherfrom the same family with kwashiorkor, and what isthe precise pathogenesis of the so called post-enteritissyndrome, remain unanswered.

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